« Previous AbstractImpacts of artificial light on food intake in invasive toads    Next AbstractEnabling liquid vapor analysis using synchrotron VUV single photon ionization mass spectrometry with a microfluidic interface »

Nature

Title:		Bacteriocin production augments niche competition by enterococci in the mammalian gastrointestinal tract
Author(s):		Kommineni S; Bretl DJ; Lam V; Chakraborty R; Hayward M; Simpson P; Cao Y; Bousounis P; Kristich CJ; Salzman NH;
Address:		"Division of Gastroenterology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. Division of Quantitative Health Sciences, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA"
Journal Title:		Nature
Year:		2015
Volume:		20151019
Issue:		7575
Page Number:		719 - 722
DOI:		10.1038/nature15524
ISSN/ISBN:		1476-4687 (Electronic) 0028-0836 (Print) 0028-0836 (Linking)
Abstract:		"Enterococcus faecalis is both a common commensal of the human gastrointestinal tract and a leading cause of hospital-acquired infections. Systemic infections with multidrug-resistant enterococci occur subsequent to gastrointestinal colonization. Preventing colonization by multidrug-resistant E. faecalis could therefore be a valuable approach towards limiting infection. However, little is known about the mechanisms E. faecalis uses to colonize and compete for stable gastrointestinal niches. Pheromone-responsive conjugative plasmids encoding bacteriocins are common among enterococcal strains and could modulate niche competition among enterococci or between enterococci and the intestinal microbiota. We developed a model of colonization of the mouse gut with E. faecalis, without disrupting the microbiota, to evaluate the role of the conjugative plasmid pPD1 expressing bacteriocin 21 (ref. 4) in enterococcal colonization. Here we show that E. faecalis harbouring pPD1 replaces indigenous enterococci and outcompetes E. faecalis lacking pPD1. Furthermore, in the intestine, pPD1 is transferred to other E. faecalis strains by conjugation, enhancing their survival. Colonization with an E. faecalis strain carrying a conjugation-defective pPD1 mutant subsequently resulted in clearance of vancomycin-resistant enterococci, without plasmid transfer. Therefore, bacteriocin expression by commensal bacteria can influence niche competition in the gastrointestinal tract, and bacteriocins, delivered by commensals that occupy a precise intestinal bacterial niche, may be an effective therapeutic approach to specifically eliminate intestinal colonization by multidrug-resistant bacteria, without profound disruption of the indigenous microbiota"
Keywords:		"Animals Bacteriocins/*biosynthesis/genetics Conjugation, Genetic/genetics Disease Models, Animal Drug Resistance, Multiple, Bacterial/genetics Enterococcus faecalis/genetics/growth & development/metabolism/*physiology Gastrointestinal Tract/*microbiology;"
Notes:		"MedlineKommineni, Sushma Bretl, Daniel J Lam, Vy Chakraborty, Rajrupa Hayward, Michael Simpson, Pippa Cao, Yumei Bousounis, Pavlos Kristich, Christopher J Salzman, Nita H eng R01 AI081692/AI/NIAID NIH HHS/ AI097619/AI/NIAID NIH HHS/ R01 AI057757/AI/NIAID NIH HHS/ R21 AI057757/AI/NIAID NIH HHS/ AI057757/AI/NIAID NIH HHS/ R01 GM099526/GM/NIGMS NIH HHS/ R21 AI097619/AI/NIAID NIH HHS/ AI081692/AI/NIAID NIH HHS/ DP2 OD006447/OD/NIH HHS/ GM099526/GM/NIGMS NIH HHS/ OD006447/OD/NIH HHS/ Research Support, N.I.H., Extramural England 2015/10/20 Nature. 2015 Oct 29; 526(7575):719-22. doi: 10.1038/nature15524. Epub 2015 Oct 19"